Comment on: “Dulaglutide treatment results in effective glycaemic control in latent autoimmune diabetes in adults (LADA): A post‐hoc analysis of the AWARD‐2, −4 and −5 trials”

Abstract

We note with interest the recent investigation by Pozzilli et al. 1 on dulaglutide treatment response in latent autoimmune diabetes in adults in the AWARD-2, −4 and − 5 trials. The authors reported no association between glutamic acid decarboxylase (GAD) islet autoantibody positivity and dulaglutide response in their combined cohort population. This is in contrast to our previously published findings in a prospective observational cohort of participants receiving other glucagon-like peptide-1 (GLP-1) receptor agonists, where glycaemic response in GAD-positive participants was reduced. 2 As noted by Pozzilli et al. the cohorts were very different; in our cohort diabetes was more severe, of longer duration and poorly controlled, islet antigen-2 autoantibodies were measured in addition to GAD, and islet autoantibody positivity was associated with severe insulin deficiency, with most autoantibody-positive participants being insulintreated, with C-peptide levels in the Type 1 diabetes range. This is consistent with studies in Type 1 diabetes, where minimal glycaemic response to GLP-1 receptor agonists is seen, except in participants Conflict of interestNone declared.

Response to the comment on: “Dulaglutide treatment results in effective glycaemic control in latent autoimmune diabetes in adults (LADA): A post‐hoc analysis of the AWARD‐2, ‐4 and ‐5 trials”

“…Jones and McDonald have misread the assay specificity of our GADA assay; their assay specificity is 97.5% and ours, based on the international workshop (DASP), is 99%; therefore, our assay is more specific than theirs . In addition, the positive predictive value of an assay increases as the population under test is enriched, as with the adult‐onset diabetes cases we studied .…”